In humans, combinations of CD4 and CXCR4 or CCR5 can mediate cell entry of HIV-1.
CPMV was previously shown to interact with vimentin displayed on cell surfaces to mediate cell entry, but the expression of surface vimentin on APCs has not been characterized.
Citric acid works in a similar manner to acetic acid, inducing the low pH transition in the viral HA protein thus rendering it unable to mediate cell entry.
Until recently, however, the mechanisms responsible for mediating cell cycle entry in primary MM cells were not known.
In line with the importance of the relative levels of the CyclinD-CDK partners in mediating cell cycle entry and progression (Sherr and Roberts, 2004), our data indicate that the presence of CDK6 in ST-HSC is sufficient to place these cells in the "starting blocks" for division upon mitogenic signaling.
The HIV-1 envelope glycoprotein (Env) trimer mediates cell entry and is conformationally dynamic1,2,3,4,5,6,7,8.
These result provide insight into mechanisms of C-peptide inhibiton of Ebola virus GP-mediated cell entry.
The envelope glycoproteins (Env) of HIV-1 mediate cell entry through fusion of the viral envelope with a target cell membrane.
The mechanism by which Tat mediates cell entry has been a focus of interest, and it has been shown that the entry mediated by Tat-PTD is not dependent on a specific receptor, energy generation or endocytosis [ 27].
We and others have shown previously that in addition to its well-characterised role in mediating cell survival, PI3K is essential for mediating cell cycle entry and expression of D-type cyclins in B-lineage cells.
